Effect of uranyl ion on liposome peroxidation and characterization of uranyl-desferrioxamine B complex

Use of depleted uranium (DU) in military armor and munitions caused potentially frequent and widespread exposure to uranium. Uranium is known to destroy the renal tubular cells, but the mechanism is not clear. Complexation of uranium with various ligands has been studied to find a chelating agent for uranium poisoning. Desferrioxamine B is a siderophore produced by Streptomyces pilosus and currently used as a chelating agent for iron poisoning. Desferrioxamine has three bidentate hydroxamic acid groups, which make six possible coordination sites for metal complexation. This study was carried out to determine whether uranyl ion promotes lipid peroxidation of lecithin liposomes and to characterize the complex between uranyl and desferrioxamine. Disappearance of the -OH peak at 3325 cm-1 in FT-IR suggests that all hydroxamic acid groups bind to uranyl ion at neutral pH. The carbonyl peak of the hydroxamic acid groups shifted from 1624 cm-1 to one broad peak at 1595 cm-1 in the complex suggesting involvement of the carbonyl oxygen in binding with uranyl ion. 1H NMR of the complex shows a decrease in the area under the curve for hydroxamic acid protons which supports FT-IR results. UV-Visible and potentiometric titration data suggest that two different species of uranyl-desferrioxamine. UO 2(H2DFO) occurs by removing two hydroxamic acid protons from the ligand below pH 5.5, where H4DFO is fully protonated DFO in the methylsulfonate salt. A third proton from the ligand is removed at pH 5.5 to 8.0 to form [UO2(HDFO)]-. There is no evidence to support uranyl-induced peroxidation of liposomes in the presence or absence of sugars and ascorbic acid. Uranyl increased hydroxyl radical formation in sugar solutions with MES buffer, but did not affect radical formation in acetate, HEPES and phosphate buffers.